Identifying a pronated foot type prior to training may help reduce the incidence of medial tibial stress syndrome by early intervention to control abnormal pronation. Findings of a higher incidence of medial tibial stress syndrome among female recruits require further investigation.

No abstract

The most commonly consumed shellfish species produced in Scotland - mussels, oysters and scallops - were investigated for the occurrence of a range of brominated and chlorinated contaminants in order to establish current levels and estimate human dietary exposure. Flesh from individual sub-samples was representatively pooled and 35 composites were analysed for brominated and chlorinated dioxins (PBDD/Fs, PCDD/Fs), brominated and chlorinated biphenyls (PBBs, PCBs), polybrominated diphenyl ethers (PBDEs), hexabromocyclododecanes (HBCDs) and tetrabromobisphenol A (TBBPA). The analytical methodology used (13)C(12) labelled surrogates of the target compounds, with GC coupled to (usually) high resolution MS, and LC-MS/MS for HBCD and TBBPA analysis. Positive identifications were made in the majority of samples for most analytes with the exception of TBBPA and most PBDD congeners measured. None of the levels detected for PCDD/F and PCB were above the maximum permitted levels specified in European Union regulations. The levels of brominated furans predominated over brominated dioxins, reflecting the environmental distribution and source emission profiles of these contaminants, and relatively high levels of the tri-brominated congeners were observed. Levels of the flame retardant chemicals reflected current and legacy use, with appreciable concentrations of PBDEs and HBCDs (predominantly alpha-HBCD) but far lower levels of PBBs. TBBPA was not detected in any of the species. In general, mussels and oysters displayed relatively higher levels of contamination than scallops, although the gonad tissue of the latter showed significant levels of brominated dioxins. The estimated adult dietary intakes of PCDD/Fs and PCBs arising from the consumption of a typical portion of these foods in combination with an otherwise average UK diet were in the range 0.5-0.6 pg World Health Organisation (WHO)-toxic equivalent (TEQ)(2005)/kg bodyweight per day. These estimated dietary intakes are well within the Tolerable Daily Intake for dioxins and dioxin-like PCBs of 2 pg WHO-TEQ(2005)/kg bodyweight/day endorsed by the independent expert Committee on Toxicology of Chemicals in Food, Consumer Products and the Environment. The corresponding intakes for sumPBDEs and sumHBCDs were 5.6-6.1 and 5.9-7.9 ng/kg bodyweight/day respectively.

It has been reported that fetal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes defects in the male reproductive system of the rat. We set out to replicate and extend these effects using a robust experimental design. Groups of 75 (control vehicle) or 55 (50, 200, or 1000 ng of TCDD/kg bodyweight) female Wistar(Han) rats were exposed to TCDD on gestational day (GD)15, then allowed to litter. The high-dose group dams showed no sustained weight loss compared to control, but four animals had total litter loss. Pups in the high-dose group showed reduced body weight up till day 21, and pups in the medium dose group showed reduced body weight in the first week postpartum. Balano-preputial separation was significantly delayed in the high-dose group male offspring. There were no significant effects of treatment when the offspring were subjected to a functional observational battery or mated with females to assess reproductive capability. Twenty-five males per group were killed on postnatal day (PND) 70, and approximately 60 animals per group (approximately 30 for the high-dose group) on PND120 to assess seminology and other end points. At PND120, the two highest dose groups showed a statistically significant elevation of sperm counts, compared to control; however, this effect was small (approximately 30%), within the normal range of sperm counts for this strain of rat, was not reflected in testicular spermatid counts nor PND70 data, and is therefore postulated to have no biological significance. Although there was an increase in the proportion of abnormal sperm at PND70, seminology parameters were otherwise unremarkable. Testis weights in the high-dose group were slightly decreased at PND70 and 120, and at PND120, brain weights were decreased in the high-dose group, liver to body weight ratios were increased for all three dose groups, with an increase in inflammatory cell foci in the epididymis in the high-dose group. These data show that TCDD is a potent developmental toxin after exposure of the developing fetus but that acute developmental exposure to TCDD on GD15 caused no decrease in sperm counts.

We have investigated whether fetal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes defects in the male reproductive system of the rat using chronically exposed rats to ensure continuous exposure of the fetus. Five- to six-week-old rats were exposed to control diet, or diet containing TCDD, to attain an average dose of 2.4, 8, and 46 ng TCDD/kg/day for 12 weeks, whereupon the rats were mated and allowed to litter; rats were switched to control diet after parturition. Male offsprings were allowed to develop until kills on PND70 (25 per group) or PND120 (all remaining animals). Offspring from the high-dose group showed an increase in total litter loss, and the number of animals alive on postnatal day (PND)4 in the high-dose group was approximately 26% less than control. The high and medium dose offsprings showed decreased weights at various ages. Balano-preputial separation (BPS) was significantly delayed in all three dose groups compared to control. There were no significant effects of maternal treatment when the offsprings were subjected to a functional observational battery or learning tests, with the exception that the high-dose group showed a deficit in motor activity. Twenty rats per group were mated to females, and there were no significant effects of maternal treatment on the fertility of these rats or on the F1 or F2 sex ratio. Sperm parameters at PND70 and 120 showed no significant effect of maternal treatment, with the exception that there was an increase in the proportion of abnormal sperm in the high-dose group at PND70; this is associated with the developmental delay in puberty in this dose group. There were no remarkable findings of maternal treatment on organ weights, with the exception that testis weights were reduced by approximately 10% at PND70 (but not PND120), and although the experiment was sufficiently powered to detect small changes, ventral prostate weight was not reduced. There were no significant effects of maternal treatment upon histopathological comparison of high-dose and control group organs. These data confirm that developmental exposure to TCDD shows no potent effect on adult sperm parameters or accessory sexual organs, but show that delay in BPS occurs after exposure to low doses of TCDD, and this is dependent upon whether TCDD is administered acutely or chronically.